Therapeutic effects of local delivery of dexamethasone on experimental brain tumors and peritumoral brain edema

1993 ◽  
Vol 79 (5) ◽  
pp. 716-721 ◽  
Author(s):  
Yukio Ikeda ◽  
Benjamin S. Carson ◽  
Jeremy A. Lauer ◽  
Donlin M. Long
Keyword(s):  
Brain Tumors ◽  
Brain Edema ◽  
Tumor Volume ◽  
Osmotic Pump ◽  
Therapeutic Modality ◽  
Therapeutic Effects ◽  
Content Type ◽  
Treatment Groups ◽  
Experimental Brain Tumors ◽  
Dexamethasone Therapy

✓ To determine if dexamethasone administered by osmotic pump directly to brain tumors would control peritumoral edema and at the same time suppress tumor growth and prolong survival, the authors studied experimental brain tumors produced in 102 rabbits by implanting VX2 carcinoma cells. Of these, 58 animals were separated into three treatment groups: Group 1 included 15 untreated rabbits; Group 2 included 18 rabbits treated with systemic dexamethasone (4 mg/kg/day); and Group 3 included 25 rabbits treated with local dexamethasone (0.24 mg/day) delivered by osmotic pump. Systemic or local dexamethasone was administered from Day 3 or Day 7 after tumor implantation, and animals were sacrificed on Day 13. A survival study was performed with 44 rabbits separated into the same treatment groups, beginning drug delivery on Day 7. Brain water content in the white matter of sacrificed animals was measured by the specific gravity method. The length and width of the brain tumors in all animals were measured and the tumor volume estimated. Findings showed that systemic and local dexamethasone administered from Day 3 or Day 7 was associated with a significant (5% level) inhibition of tumor volume as well as a mean reduction of brain edema in most tested sites. Systemic and local dexamethasone therapy also resulted in a significant (5% level) increase in survival time relative to the untreated group. These short-term results suggest that locally delivered dexamethasone may constitute a clinically important therapeutic modality.

scholarly journals Therapeutic effects of topical dexamethasone on experimental brain tumors and peritumoral brain edema.

1992 ◽  
Vol 7 (2) ◽  
pp. 143-145
Author(s):  
Yukio Ikeda ◽  
Shozo Nakazawa ◽  
Benjamin S. Carson ◽  
Donlin M. Long
Keyword(s):  
Brain Tumors ◽  
Brain Edema ◽  
Therapeutic Effects ◽  
Experimental Brain Tumors ◽  
Peritumoral Brain Edema

Avascular necrosis of bone following short-term dexamethasone therapy for brain edema

1984 ◽  
Vol 61 (5) ◽  
pp. 983-985 ◽  
Author(s):  
Avital Fast ◽  
Malvina Alon ◽  
Shmuel Weiss ◽  
Freddy R. Zer-Aviv
Keyword(s):  
Brain Edema ◽  
Avascular Necrosis ◽  
Joint Destruction ◽  
Steroid Treatment ◽  
Bone Scanning ◽  
Short Term ◽  
Content Type ◽  
Dexamethasone Therapy ◽  
Avascular Necrosis Of Bone ◽  
Fine Print

✓ The authors present a case of avascular necrosis of both femoral and humeral heads which developed after short-term steroid treatment for brain edema. Avascular necrosis of bone may develop after short-term as well as after maintenance steroid therapy. Early diagnosis with bone scanning and management may in some cases prevent joint destruction.

The importance of pial blood supply to the development of peritumoral brain edema in meningiomas

1997 ◽  
Vol 87 (3) ◽  
pp. 368-373 ◽  
Author(s):  
Michael Bitzer ◽  
Lars Wöckel ◽  
Andreas R. Luft ◽  
Ajay K. Wakhloo ◽  
Dirk Petersen ◽  
...  
Keyword(s):  
Brain Edema ◽  
Blood Supply ◽  
Tumor Volume ◽  
Volume Ratio ◽  
Content Type ◽  
Total Tumor Volume ◽  
Pial Vessels ◽  
Peritumoral Brain Edema ◽  
Tumor Region ◽  
The Mean

✓ In a retrospective analysis, the authors studied the pial and dural blood supplies in 74 intracranial meningiomas and quantified their associated peritumoral brain edema (PTBE). The extent and localization of pial blush in relation to the total tumor volume were determined angiographically. The amount of edema and tumor size were calculated using computerized tomography. The edema—tumor volume ratio was defined as Edema Index (EI). There were 49 meningiomas with PTBE; of those tumors, 46 were supplied by pial vessels, and three were supplied exclusively by dural vessels. Tumors without PTBE showed no pial blush. The mean EI in meningiomas with pial blush was significantly larger (EI = 3) than in meningiomas without pial supply (EI = 1.1; p < 0.0001). Meningiomas with a smaller pial supply than dural supply had a significantly smaller mean EI than tumors with a pial supply equal to or greater than the dural supply (EI = 2.9 vs. EI = 3.7; p < 0.015). In 69.9% of cases with pial blood supply, major portions of the edema were located adjacent to the tumor region supplied by pial vessels. Edema index differences among tumors of different subgroups, as defined by size or histology, were significantly related to the pial supply in each subset. Thus, pial blood supply may be associated with the development of PTBE in meningiomas.

Effect of the antiprogesterone RU-38486 on meningioma implanted into nude mice

1987 ◽  
Vol 66 (4) ◽  
pp. 584-587 ◽  
Author(s):  
Jeffrey J. Olson ◽  
David W. Beck ◽  
Janet A. Schlechte ◽  
Pao-Min Loh
Keyword(s):  
Tumor Growth ◽  
Nude Mice ◽  
Binding Proteins ◽  
Tumor Volume ◽  
Growth Index ◽  
Control Group ◽  
Content Type ◽  
Treatment Groups ◽  
Steroid Binding Proteins

✓ Meningiomas have been shown to have steroid-binding proteins. In vitro, estradiol, progesterone, and the antiestrogen tamoxifen stimulate tumor growth. However, incubation of tumor cells with an antiprogesterone agent results in tumor inhibition. In this investigation, a human meningioma was implanted subcutaneously in athymic nude mice. Two treatment groups were established, one receiving the antiprogesterone agent RU-38486 (10 mg/kg/day in suspension) and the other receiving only vehicle. After 3 months, the tumor growth index (defined as the tumor volume at 3 months divided by the initial tumor volume) was 0.25 ± 0.46 (mean ± standard deviation) in the group receiving antiprogesterone and was 1.54 ± 0.58 in the control group (p = 0.041). Further investigation of the effect of antiprogestational agents on the growth and hormone-binding proteins of other meningiomas will better define the mechanism of their effects.

Regional metabolism in experimental brain tumors in cats: relationship with acid/base, water, and electrolyte homeostasis

1992 ◽  
Vol 77 (6) ◽  
pp. 917-926 ◽  
Author(s):  
Yoshikazu Okada ◽  
Otmar Kloiber ◽  
Konstantin A. Hossmann
Keyword(s):  
Brain Tumors ◽  
Tumor Tissue ◽  
Atp Depletion ◽  
Resonance Spectroscopy ◽  
Peritumoral Edema ◽  
Metabolic Pattern ◽  
Tissue Ph ◽  
Content Type ◽  
Experimental Brain Tumors ◽  
Fine Print

✓ Experimental brain tumors were produced in cats by xenotransplantation of the rat glioma clone F98 into the white matter of the left hemisphere. One to 4 weeks after implantation, local adenosine triphosphate (ATP), glucose, lactate, and tissue pH were measured via imaging techniques in cryostat sections passing through the center of the tumor and correlated with changes in water and electrolyte content. The tumors exhibited a heterogeneous metabolic pattern, with a tendency for ATP to decrease and lactate to increase during tumor development. Tissue pH was above 7.5 in tumors with high ATP content but it sharply declined at low ATP levels. In peritumoral edema, ATP also decreased and lactate increased but, in contrast to tumor tissue, pH became more alkaline. Metabolic changes were associated with edema formation, as evidenced by the rise in water and sodium content. There was a distinct difference between tumor tissue and peritumoral edema: in tumor tissue, pH declined with increasing water content, whereas in peritumoral edema it increased. These observations are interpreted as follows: 1) in tumor tissue, “lactacidosis” and ATP depletion are attributed to disturbances in blood flow, resulting in metabolic failure and the intracellular “cytotoxic” accumulation of water; 2) in peritumoral edema, “lactalkalosis” is the result of an efflux of (alkaline) lactate salts from the tumor into the expanded extracellular compartment, and the decrease in ATP is the volumetric effect of extracellular “vasogenic” edema fluid and not the result of cellular energy failure. These findings are of importance for the interpretation of volume-selective magnetic resonance spectroscopy and may contribute to the establishment of spectroscopic criteria for the evaluation of therapeutical interventions.

Acetazolamide therapy for symptomatic plateau waves in patients with brain tumors

2002 ◽  
Vol 97 (1) ◽  
pp. 224-226 ◽  
Author(s):  
Christopher J. Watling ◽  
J. Gregory Cairncross
Keyword(s):  
Intracranial Pressure ◽  
Carbonic Anhydrase ◽  
Brain Tumors ◽  
Neurological Disorder ◽  
Malignant Gliomas ◽  
Effective Therapy ◽  
Content Type ◽  
Plateau Waves ◽  
Dexamethasone Therapy ◽  
Fine Print

✓ In this report, the authors describe three patients with malignant gliomas who experienced paroxysmal neurological symptoms triggered by standing. The symptoms were attributed to acute elevations of intracranial pressure, an uncommon phenomenon called “plateau waves.” In each instance, the attacks occurred despite the fact that the patient was receiving dexamethasone therapy and stopped promptly with the addition of acetazolamide. Acetazolamide, an orally administered carbonic anhydrase inhibitor, appears to be a specific and effective therapy for this uncommon neurological disorder.

Photoirradiation therapy of experimental malignant glioma with 5-aminolevulinic acid

2002 ◽  
Vol 97 (4) ◽  
pp. 970-976 ◽  
Author(s):  
Bernhard Olzowy ◽  
Cornelia S. Hundt ◽  
Susanne Stocker ◽  
Karl Bise ◽  
Hans Jürgen Reulen ◽  
...  
Keyword(s):  
Body Weight ◽  
Brain Tumors ◽  
Intravenous Administration ◽  
Aminolevulinic Acid ◽  
Cold Injury ◽  
Mr Images ◽  
Content Type ◽  
Experimental Brain Tumors ◽  
Photofrin Ii ◽  
Fine Print

Object. Accumulation of protoporphyrin IX (PPIX) in malignant gliomas is induced by 5-aminolevulinic acid (5-ALA). Because PPIX is a potent photosensitizer, the authors sought to discover whether its accumulation might be exploited for use in photoirradiation therapy of experimental brain tumors, without injuring normal or edematous brain. Methods. Thirty rats underwent craniotomy and were randomized to the following groups: 1) photoirradiation of cortex (200 J/cm2, 635-nm argon-dye laser); 2) photoirradiation of cortex (200 J/cm2) 6 hours after intravenous administration of 5-ALA (100 mg/kg body weight); 3) cortical cold injury for edema induction; 4) cortical cold injury with simultaneous administration of 5-ALA (100 mg/kg body weight) and photoirradiation of cortex (200 J/cm2) 6 hours later; or 5) irradiation of cortex (200 J/cm2) 6 hours after intravenous administration of Photofrin II (5 mg/kg body weight). Tumors were induced by cortical inoculation of C6 cells and 9 days later, magnetic resonance (MR) images were obtained. On Day 10, animals were given 5-ALA (100 mg/kg body weight) and their brains were irradiated (100 J/cm2) 3 or 6 hours later. Seventy-two hours after irradiation, the brains were removed for histological examination. Irradiation of brains after administration of 5-ALA resulted in superficial cortical damage, the effects of which were not different from those of the irradiation alone. Induction of cold injury in combination with 5-ALA and irradiation slightly increased the depth of damage. In the group that received irradiation after intravenous administration of Photofrin II the depth of damage inflicted was significantly greater. The extent of damage in response to 5-ALA and irradiation in brains harboring C6 tumors corresponded to the extent of tumor determined from pretreatment MR images. Conclusions. Photoirradiation therapy in combination with 5-ALA appears to damage experimental brain tumors selectively, with negligible damage to normal or perifocal edematous tissue.

Effect of dexamethasone on experimental brain edema in cats

1976 ◽  
Vol 45 (2) ◽  
pp. 141-147 ◽  
Author(s):  
Arthur R. Dick ◽  
Mary E. McCallum ◽  
John A. Maxwell ◽  
Stanley R. Nelson
Keyword(s):  
White Matter ◽  
Brain Edema ◽  
No Reduction ◽  
Cortical Lesions ◽  
Contralateral Hemisphere ◽  
Content Type ◽  
Deep White Matter ◽  
Dexamethasone Therapy ◽  
Experimental Brain Edema ◽  
Adult Cats

✓ The authors studied the effects of dexamethasone, 0.3 mg/kg/hr administered intravenously beginning 1 hour before injury, in adult cats with brain edema secondary to cold-induced cortical lesions. Edema was quantitatively measured in cortex, gyral white matter, and central (deep) white matter at 3, 24, 48, and 72 hours, with and without dexamethasone, by determining specific gravity (density) of samples in a continuous gradient column. Cold-induced lesions resulted in edema, which was greatest in the white matter of the injured hemisphere but also present in the contralateral hemisphere. Except for a slight but significant increase in density (decreased edema) of cortex at 24 hours, dexamethasone therapy resulted in no reduction of cold-induced edema, and in some cases increased the edema.

Gamma knife radiosurgery for craniopharyngiomas

2000 ◽  
Vol 93 (supplement_3) ◽  
pp. 47-56 ◽  
Author(s):  
Wen-Yuh Chung ◽  
David Hung-Chi Pan ◽  
Cheng-Ying Shiau ◽  
Wan-Yuo Guo ◽  
Ling-Wei Wang
Keyword(s):  
Clinical Outcome ◽  
Gamma Knife ◽  
Tumor Volume ◽  
Gamma Knife Radiosurgery ◽  
Tumor Control ◽  
Content Type ◽  
Stereotactic Aspiration ◽  
Cystic Component ◽  
The Mean ◽  
Fine Print

Object. The goal of this study was to elucidate the role of gamma knife radiosurgery (GKS) and adjuvant stereotactic procedures by assessing the outcome of 31 consecutive patients harboring craniopharyngiomas treated between March 1993 and December 1999. Methods. There were 31 consecutive patients with craniopharyngiomas: 18 were men and 13 were women. The mean age was 32 years (range 3–69 years). The mean tumor volume was 9 cm3 (range 0.3–28 cm3). The prescription dose to the tumor margin varied from 9.5 to 16 Gy. The visual pathways received 8 Gy or less. Three patients underwent stereotactic aspiration to decompress the cystic component before GKS. The tumor response was classified by percentage reduction of tumor volume as calculated based on magnetic resonance imaging studies. Clinical outcome was evaluated according to improvement and dependence on replacement therapy. An initial postoperative volume increase with enlargement of a cystic component was found in three patients. They were treated by adjuvant stereotactic aspiration and/or Ommaya reservoir implantation. Tumor control was achieved in 87% of patients and 84% had fair to excellent clinical outcome in an average follow-up period of 36 months. Treatment failure due to uncontrolled tumor progression was seen in four patients at 26, 33, 49, and 55 months, respectively, after GKS. Only one patient was found to have a mildly restricted visual field; no additional endocrinological impairment or neurological deterioration could be attributed to the treatment. There was no treatment-related mortality. Conclusions. Multimodality management of patients with craniopharyngiomas seemed to provide a better quality of patient survival and greater long-term tumor control. It is suggested that GKS accompanied by adjuvant stereotactic procedures should be used as an alternative in treating recurrent or residual craniopharyngiomas if further microsurgical excision cannot promise a cure.

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